DIFFERENTIAL EXPRESSION OF GENES REGULATED BY THE GLUCOCORTICOID RECEPTOR IN PATIENTS WITH PULMONARY TUBERCULOSIS.

GALLUCCI GEORGINA; IMHOFF MATILDE; FERNANDEZ ROCIO DEL VALLE; DIAZ ARIANA; BONGIOVANNI BETTINA; SANTUCCI NATALIA; BÉRTOLA DIEGO; GARDEÑEZ WALTER; BAY MARÍA LUISA; BOTTASSO OSCAR; DATTILIO LUCIANO

Tucumán

Congreso; Congreso LXVII de SAI; 2019

SAI

Tuberculosis is the mainly cause of death among infectious diseases. Our earlier studies in patients with pulmonary (TB) showed the presence of an immuno-endocrine imbalance characterized by a disease-severity associated increase in plasma levels of proinflammatory cytokines, cortisol and the cortisol/DHEA ratio, without changes in the expression of the functional isoform of the glucocorticoid receptor (GRα). Extending these findings, we now investigated the expression of GR-regulated genes (RT-qPCR) mostly involved in the down-modulation of the immune response (AnxA1, FKBP5, GILZ, NFKBIBα and NFKBIBβ), in peripheral blood mononuclear cells from adult TB patients, HIV negative (n=47) and healthy controls (HCo, n=47). Transcript levels of AnxA1 (p=0.006), GILZ (p=0.033) and NFKBIBβ (p=0.041) mRNA appeared significantly increased in TB patients respect to HCo, whereas the expression of FKBP5 and NFKBIBα remained unchanged. Upon analyzing according to disease severity, mRNA for AnxA1 (p=0.006) and NFKBIBβ (p=0.025) were higher in moderate and severe TB if compared to HCo; with GILZ and NFKBIBα appearing increased in moderate and severe, respectively (p